Physio EKG II/Cardiac Muscle Mechanics (15/16)

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Physio EKG II/Cardiac Muscle Mechanics (15/16)
2014-02-09 12:52:12
MBS Physiology
Exam 2
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  1. Lecture 15 - EKG II
  2. What heart disease affects/prolongs the P-R interval on an EKG?
    heart block
  3. Heart Block
    a blockage at any level of the electrical conduction system of the heart
  4. First-degree AV Block (PR prolongation)
    • occurs when a signal from the SA node is delayed & travels slower than normal b/c of some block in the AV node
    • the P-wave conducts to a QRS but the PR interval increases to more than 0.20 seconds
  5. Mobitz Type I Heart Block
    • • characterized by PR intervals that become progressively longer on consecutive beats followed by a blocked P wave (a 'dropped' QRS complex)
    • • after the dropped QRS complex the PR interval resets & the cycle repeats
    • • goes PR normal → longer → longer → missed beat
    • • almost always a disease of the AV node

    • synonyms: Type 1 Second-degree AV block, Wenckebach Periodicity
  6. Mobitz Type II Heart Block (Type 2 Second-degree AV block)
    • • characterized by intermittently non-conducted P waves (missed beats)
    • • there's NO lengthening or shortening of the PR interval
    • • the PR intervals don't change; some but not all P waves conduct to ventricles

  7. Third-degree AV Block (Complete Heart Block)
    • • impulses generated in the SA node in the atrium don't propagate to the ventricles - there's no electrical connection between SA & AV node
    • • none of the P waves conduct to the ventricles
    • • on the EKG there's no apparent relationship between P waves & QRS complexes - the atria & ventricles beat independently

  8. Complete Heart Block Symptoms
    • the SA node determines the rate of P waves while the ventricular pacemaker sets an underlying ventricular rhythm (slow: 40-50 bpm)
    • low cardiac output b/c there's no atrial kick
    • bradycardia (slowed heart rate)
    • hypotension
    • hemodynamic instability
    • treated w/ a pacemaker
  9. What heart disease affects the QRS complex?
    bundle branch blocks
  10. Bundle Branch Blocks
    • when a bundle branch fails to conduct electrical impulses appropriately (due to injury, heart disease, MI, surgery) there is an altered (prolonged) pathway for ventricular depolarization
    • results in an abnormally long QRS complex
    • the rapid spread of an AP is compromised - signal will travel down as far as possible, then around an area of damage
    • rapid conduction velocity is lost
  11. When does an "irregularly irregular" rhythm occur?
    • Atrial Fibrillation: is unpredictable & chaotic w/ no underlying rhythm
    • (worms)
  12. Atrial Fibrillation
    lacks normal P waves; instead F (fibrillation) waves are seen & caused by multiple coexisting wavelets that circulate within the atria & produce rapid stimulation of the AV node

    myocardial cells in the atrium might start to become hyperexcitable ectopic focci of SA node

    those depolarizations, which conduct to the ventricles, produce normal QRS complexes since they originated in the atria

    the irregular rhythm results in variable filling time & therefore variable pulse pressure & cardiac output

    • top (red arrow) = A.fib
  13. Ventricular Fibrillation
    • an EKG shows completely irregular chaotic deflections of varying amplitude, width, & shape
    • ectopic focci would mostly be in ventricle
    • causes cardiac arrest & is often a terminal event b/c cardiac output is essentially zero due to weak, uncoordinated ventricular contractions
  14. What is the difference between a SA node block & a SA node suppression?
    • in SA node block an electrical impulse is generated by the SA node that doesn't make the atria contract
    • IN SA node suppression, the SA node doesn't generate an electrical impulse b/c it is reset by the electrical impulse that enters the SA node
  16. Lecture 16 - Cardiac Muscle Mechanics
  17. Isotonic Contraction
    • shortening occurs
    • used to investigate the velocity of shortening against various loads
  18. Isometric Contraction
    • no shortening occurs because afterload is too large
    • used to investigate the generation of force at varying rest lengths
  19. Preload
    • the force which acts to stretch a muscle prior to its contraction (determines its length before it begins to contract)
    • related to how much blood fills ventricles before the muscle contracts
    • a change in preload means a change in stroke volume
  20. Afterload
    • the load against which a muscle tries to shorten
    • the tension or stress developed in the wall of the left ventricle during ejection
    • can be broken into components: aortic pressure + the pressure the ventricle must overcome to eject blood
  21. The _______ the Aortic/pulmonary pressure, the _______ the afterload on the Left/right ventricle.
  22. Contractility
    • ability of the heart to develop force (to contract)
    • can be affected by chemical (ionotropic) agents
  23. What is the relationship between myocyte rest length & Ca2+ sensitivity?
    • the more stretched a cell is, the more sensitive it is to Ca2+ concentrations
    • when a sarcomere length is increased, LESS Ca2+ is needed to produce 50% of maximal force
    • (caused by an increased sensitivity of contractile proteins to Ca2+ with stretch)
  24. Starling’s Law of the Heart
    • the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (end diastolic volume)
    • the increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully
    • when "filling pressure" is increased, ventricular end diastolic pressure & end diastolic volume increases
    • a stretched ventricle develops greater contractile force & peak ventricular pressure + a greater stroke volume
    • (the greater the diastolic stretch, the larger the resulting stroke volume)
    • applies to INTACT cardiovascular systems in animals & humans
  25. β Agonist or Antagonist Effects on Starling Relationship
    • • epinephrine (β agonist) shifts the Starling curve upward so that at each rest length there's increased active force/contraction of the heart
    • • curve represents a “positive inotropic” effect, there is increased “contractility”, & EPI is a “positive inotrope”

    • • propranolol (a β antagonist) depresses active force development at each rest length
    • • represents a “negative inotropic” effect, decreased “contractility”, & propranolol is a “negative inotrope”

  26. Velocity of Shortening
    • the recorded velocity of a muscle shortening when it is attached to a load it can lift
    • in vivo analogy: measuring ventricle ejection rate (velocity of shortening) at different aortic pressures (afterloads)
  27. Relationship Between Velocity of Shortening & Afterload (P)
    • as afterload increases, the velocity of shortening decreases
    • stroke volume decreases as afterload INCREASES
    • therefore on the graph, stroke volume could be substituted for velocity of shortening & aortic pressure could be substituted for afterload
  28. Vmax Velocity of Shortening
    the fastest possible velocity a muscle can shorten when there is no afterload opposing said muscle shortening
  29. P0
    • when the afterload is so great, the heart can no longer shorten against it
    • at this point the ventricle is still contracting, but because the afterload/resistance in the aorta is so great, it becomes an isometric contraction
    • to the left of P0 contractions are isotonic; to the right of P0 contractions are isometric
  30. Effects of a More Optimum Rest Length on Afterload Velocity Relationship
    • at any given preload, increasing the afterload decreases velocity of contraction thereby decreasing stroke volume
    • however that effect can be mitigated by starting with a greater rest length aka filling the ventricle more aka having a higher end diastolic volume
  31. What is the only value not affected by rest length?
    • Vmax
    • stays the same no matter how the rest length is varied
    • i.e. a greater rest length leads to a greater velocity of shortening against increasing afterloads, however Vmax stays the same no matter what the rest length is
  32. Besides rest length, what is another variable that can change the velocity of shortening against an increasing afterload?
    • a β agonist (eg. NE or EPI)
    • velocity of shortening is protected against the effects of a large afterload in the presence of sympathetic stimulation/β agonism
    • *causes an increase in both Vmax & P0 (the increase in Vmax indicates a positive inotropic effect)
  33. Heterometric Regulation of Myocardial Function
    • heterometric changes are brought about by changes in rest length (preload)

    • include increases in force of contraction, peak ventricular pressure, & stroke volume but NOT maximum velocity of shortening (Vmax)

    • are thought to be due to changes in the number of myosin cross-bridges interacting in a given contraction
  34. Homeometric Regulation of Myocardial Function
    • homeometric changes occur w/out changes in rest length

    • are brought about by changes in sympathetic stimulation

    • produce changes in both Vmax & P0

    • are thought to result from changes in cross bridge cycling rate (increases in cross bridge cycling rate result in a greater number of cross bridge interactions which also increase P0)
  35. How can effects of ionotropic agents be described?
    as Homeometric in that they are NOT dependent on a change in rest length
  36. Overall Effects of Venous Return & Inotropy on Cardiac Output
    • ↑ venous return → ↑ COs
    • ↓ venous return → ↓ COs
    • ↑ inotropy → ↑ COs (SNS stimulation)
    • ↓ inotropy → ↓ COs
  37. → ↑ → ↓ •